Tissue

Stores fat and houses most of the body's aromatase, so more fat mass means more conversion of androgen to estrogen.

Makes cortisol and the adrenal androgens. It answers to ACTH from the pituitary, which is why shutting down the testicular axis leaves it running.

The threat detector. Dense in androgen receptors, and the structure most implicated in the anger, vigilance and fear side of what these compounds do. Splitting it out of the limbic system matters because threat processing and reward processing sit in the same blob otherwise, and compounds pull them in opposite directions.

Where conflict is detected and effort is allocated. In long-term users this region shows a chemical signature of altered glutamate handling, which is the closest thing in the human literature to direct evidence of a neurotoxic process.

The gland that actually releases growth hormone, LH and FSH. Every GH secretagogue and every GnRH drug is aimed here, upstream of the tissue where the effect is finally felt.

The support cell that feeds neurons and clears glutamate from the synapse. It also expresses aromatase, which means part of the brain's own estrogen supply comes from glia.

The structure behind sustained, undirected dread, as opposed to the sharp fear the amygdala produces. It matters here because the anxiety reported after a cycle is usually the slow kind with no object, which is this structure.

What decides whether a compound in the blood reaches the brain at all. It is the reason two drugs with the same target can have completely different mental effects: one crosses and one does not.

Where red cells are built. Androgens push it harder, which is why they were once a treatment for anaemia and why haematocrit climbs on cycle.

Responds to both estrogen and prolactin. Once glandular tissue forms it does not go away on its own, which is why this one is worth preventing early.

The lining of the airways. It is the target of the lung bioregulators and one of the tissues VIP acts on.

Joint surface tissue with almost no blood supply, which is why it repairs so slowly and why it is targeted separately from tendon.

Coordination and timing, and increasingly recognised as carrying part of cognitive processing speed as well as movement. Included because motor slowing shows up in the drug literature on anti-estrogens and has nowhere else to point.

The wiring between the processors. It carries the speed at which regions can talk to each other, so damage here presents as slowness and poor coordination between functions.

The one part of the adult human brain where new neurons are reliably born. It sits at the entrance to the hippocampus, which is why anything that suppresses neurogenesis shows up first as a memory complaint.

Where a repeated action stops being a choice and becomes a habit. Relevant because the transition from using a compound deliberately to using it by default is a real neural change.

The single cell layer separating gut contents from the bloodstream. Most peptides sold for gut health are aimed at either repairing it or keeping its tight junctions shut.

Carries androgen receptors like skeletal muscle does, and thickens under the same signal. Unlike a bicep, a thicker left ventricle fills less well.

Where new memory is laid down. Unusually sensitive to sustained cortisol and to lost deep sleep, both of which these compounds can produce, which makes it the structure behind most reported memory complaints.

The control room above the pituitary. Appetite, body temperature, the reproductive axis and the GH rhythm are all set here, which is why so many peptides that produce whole-body effects act on one small area.

Where the body's internal state is read and turned into a feeling. Palpitations, breathlessness and a sense that something is physically wrong are assembled here, which is why cardiovascular strain from these compounds often presents first as anxiety.

Controls sodium and water balance and produces erythropoietin, so it sits behind both the bloat and the rising red cell count.

The convergence point of the aggression circuit and the best-characterised site of a steroid effect on behaviour anywhere in the literature. Adolescent exposure changes vasopressin, dopamine, serotonin and GABA signalling here together, which is why the behaviour change is not undone by acting on any one of them.

The testicular cells that actually make testosterone in response to LH. Anything that restarts the axis has to reach these; anything that shuts the axis down starves them.

The emotional core of the brain, and androgen-receptor rich. This is where mood, threat response and aggression are set, and where steroid mental effects are thought to land.

Processes every oral steroid on first pass. The 17-alpha-alkyl group that lets an oral survive that trip is also what makes it hard on this organ.

The brain's noradrenaline source and its arousal dial. It sets how alert, how startled and how awake the person is, which is why compounds that raise sympathetic drive cost sleep before they cost anything else.

The most aromatase-rich region in the male brain. Testosterone is converted to estradiol here before it acts, which means much of what looks like an androgen effect on sexual behaviour is an estrogen effect one step downstream.

The brain's resident immune cell, and the hinge of the whole estrogen protection argument. Estrogen holds these cells in a surveilling state. Remove estrogen and they shift to an activated state and release the cytokines that damage the neurons around them.

Where reward is registered and where the decision to repeat something is made. Anabolic steroids are reinforcing in animals at this site, which is the anatomical reason dependence is possible at all.

Where the value of an outcome is weighed against its cost, and the region most consistently thinned in dependent users. This is the specific anatomy behind poor risk judgement.

The insulin and glucagon-producing cells. Incretin drugs raise insulin here only when glucose is already high, which is why they do not cause hypoglycaemia on their own the way injected insulin does.

Where a threat becomes an action: freeze, flee or attack. It receives the amygdala's alarm and executes it. Relevant here because it explains why the reported anger is sudden and physical.

The gland that makes melatonin and sets the day-night rhythm. The Russian bioregulator peptides are aimed at it on the theory that restoring that rhythm slows other ageing processes.

Planning, judgement and the brake on impulse. Relevant here because the reported behaviour change on these compounds is often better described as a weaker brake than as a stronger drive, and those two have different consequences.

Growth here is driven mainly by DHT, which is why compounds that resist 5-alpha-reductase are gentler on it.

The brain's serotonin source. It sets patience, satiety with a situation and the threshold at which irritation becomes an outburst. Adolescent steroid exposure changes serotonin signalling in animals, and the change reverses direction on withdrawal.

In a genetically susceptible scalp, DHT binding shrinks the follicle a little with each cycle. The predisposition is inherited; the androgen sets the pace.

Oil glands in the skin. Androgen signalling raises output, and heavier oil plus keratin plugging is how steroid acne starts.

The intended target. Dense in androgen receptors, and the tissue where the whole risk trade is being made.

The largest organ, and the target for the melanocortin and copper peptides. Pigment, collagen and wound repair all happen here.

Where ghrelin is produced and where GLP-1 agonists slow emptying. That slowing is both the satiety mechanism and the source of the nausea.

Connective tissue adapts far slower than muscle. A strength jump that outpaces it is the setup for a tear.

Makes testosterone and sperm, and needs LH and FSH from the pituitary to do either. Cut that signal and it shrinks and goes quiet.

Where T-cells mature. It shrinks steadily with age, which is the premise behind every thymic peptide: restore the training ground.

The single-cell lining of every blood vessel. It sets vessel tone and is where plaque begins when lipids and pressure both move the wrong way.

Where the brain's dopamine neurons live. Everything that feels rewarding, including the compounds themselves, is signalled from here. This is the origin of the reward pathway.